Division of Gastroenterology, Department of Internal Medicine, University of Indonesia, Jakarta, Indonesia.
J Dig Dis. 2013 Sep;14(9):455-62. doi: 10.1111/1751-2980.12081.
Pathogenesis of inflammatory bowel disease (IBD) remains an enigma on whether germs, genes or a combination of these two with excessive immune responses to gut-associated bacteria explicates its pathomechanisms. The incidence of IBD is 0.76747 per 100,000 in Central Indonesia, as shown in the Project Indonesian IBD ACCESS 2012 progress report. This result, together with other epidemiological studies in Asia, may conclusively reflect increased rates of the disease, while its pathogenesis still undoubtedly obscured. However, knowledge of the pathophysiology of IBD is rapidly growing, abreast with new developments. A series of recent updates in core pathomechanisms such as bacterial, endoplasmic reticulum stress, new immune cell populations, T-cell differentiation and function, mucosal immune defenses and oxidative stress are relevant pathomechanism keypoints in IBD.
炎症性肠病(IBD)的发病机制仍然是一个谜,是细菌、基因还是两者的结合,以及对肠道相关细菌的过度免疫反应解释了其发病机制。中央印度尼西亚的 IBD 发病率为每 100,000 人 0.76747,如 2012 年印度尼西亚 IBD ACCESS 项目进度报告所示。这一结果与亚洲的其他流行病学研究一起,可能最终反映出该疾病的发病率增加,而其发病机制仍然毫无疑问地不清楚。然而,IBD 的病理生理学知识正在迅速发展,与新的发展同步。最近在核心发病机制方面的一系列更新,如细菌、内质网应激、新的免疫细胞群体、T 细胞分化和功能、黏膜免疫防御和氧化应激,是 IBD 相关的发病机制关键点。